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Volume 125, Issue 5, Pages e210-e213 (May 2010)


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Parameters of the thrombogram are associated with serum 25-hydroxyvitamin D levels at baseline, but not affected during supplementation with vitamin D

Rolf JordeabCorresponding Author Informationemail address, Monica Snevec, Peter Torjesend, Yngve Figenschaue, John-Bjarne Hansenf

Received 10 November 2009; received in revised form 5 December 2009; accepted 17 December 2009. published online 22 February 2010.

Abstract 

Introduction

In vitro studies indicate an anticoagulant effect of 1,25-dihydroxyvitamin D, and sun exposure may lower the risk of thrombotic events. Accordingly, an effect on haemostatic parameters could be expected after supplementation with vitamin D.

Materials and Methods

158 obese or overweight subjects were included in a one year intervention study with supplementation with 40.000IU vitamin D3 per week or placebo. All subjects were given 500mg calcium daily. Plasminogen activator inhibitor 1 (PAI-1), tissue plasminogen activator antigen (tPA Ag), and tissue factor-induced thrombin generation over time in plasma assessed by the calibrated automated thrombogram (CAT) method as a parameter of over all thrombotic activity, were measured before and at the end of the study.

Results

Mean baseline serum 25(OH)D level was 61.8nmol/L and increased in the vitamin D group to 145.6nmol/L at the end of the study. At baseline there was a significant decrease in the CAT variables lag time and time to peak of the thrombogram across increasing serum 25(OH)D quartiles, whereas no significant associations between serum 25(OH)D and PAI-1 or tPA Ag were found. After one year, no significant differences were found between the vitamin D and placebo groups regarding change in any of the haemostatic parameters.

Conclusions

The association between lag time and time to peak in the CAT assay and serum 25(OH)D levels could indicate a pro-thrombotic state in subjects with high serum 25(OH)D levels, whereas the lack of effect of high dose vitamin D supplementation questions the causality of this relation.

a Institute of Clinical Medicine, University of Tromsø, Norway

b Medical Clinic, University Hospital of North Norway, Tromsø, Norway

c Department of Neurosurgery and Ophthalmology, Divison of Ophthalmology, University, Hospital of North Norway, 9038 Tromsø, Norway

d Hormone Laboratory, Aker University Hospital, Oslo, Norway

e Department of Medical Biochemistry, University Hospital of North Norway, and Institute of Medical Biology, University of Tromsø, Tromsø, Norway

f Center for Atherothrombotic Research in Tromsø (CART), Institute of Clinical Medicine, University of Tromsø, Tromsø, Norway

Corresponding Author InformationCorresponding author. Medical Clinic, University Hospital of North Norway, 9038 Tromsø, Norway. Tel.: +47 776 26000; fax: +47 776 26863.

PII: S0049-3848(09)00563-5

doi:10.1016/j.thromres.2009.12.011


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